Health and medical information

These drugs are used where NSAIDs have been.tried, and have failed to control the symptoms. Most have some effect on the immune response within the joint. They have the advantage of checking the progress of joint destruction caused by rheumatoid arthritis, whereas NSAIDs simply suppress the immediate effects. On the other hand, they are powerful drugs which are more likely to cause side-effects. Once they are started, they will probably have to be taken for many years. For this reason, doctors delay using them until they are sure they are necessary. If taking such drugs, it is very important to have regular medical supervision and report any side-effects to the doctor.

The drugs commonly used are: penicillamine (Distamine, Pendramine) gold salts (Myocrisin, Ridaura) sulphasalazine (Salazopyrin) hydroxychloroquine (Plaquenil)

In severe cases of rheumatoid arthritis, that do not respond to other treatments, drugs which have a general suppressive effect on the immune system may sometimes be used. The main one is azathioprine (Azamune, Imuran). These drugs make the body less able to fight infections, and at high doses they could make patients more susceptible to cancer. Corticosteroids (see Section 5) are sometimes used where none of the above treatments are effective.

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The relevance of food relationships to food sensitivity is explained on p255. Briefly, a person who is sensitive to one plant food (eg oranges) may react badly to other foods from related plants (eg lemons and grapefruit). The same also goes for foods from animal sources?

In the past, a great deal of emphasis has been placed on ‘food families’ – by those treating food intolerance. These doctors have automatically looked at the taxonomic family of plants and animals to predict when cross-reactions are likely to occur.

But the family is just one sort of group in taxonomy – the science of biological classification. A closer look at the cross-reactions shown by patients suggests that the family is not always the most relevant group to consider. Sometimes we need to consider higher or lower levels of classification. The over-emphasis on food families can create problems. For example, it can lead food-sensitive people to eat too much of some potentially troublesome foods (eg fish) while avoiding many plant foods unecessarily.

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One of the strand of the argument is more contentious and very difficult to test scientifically. It suggests that we need more nutrients than we once did, simply because our bodies have to deal with so many more toxins – pesticide residues in food and water, air pollutants and so on. Although this might seem rather far-fetched, it is not implausible. We protect our bodies against toxins by breaking them down with enzymes. Many vitamins act as coenzymes – substances that are needed by specific enzymes to help them do their work. Minerals such as zinc and magnesium are also important for enzyme function. Faced with an extra burden of toxins to destroy, perhaps we do need more vitamins and minerals than our traditional diet provides.

A related issue here is the Pill, which is said to alter the nutritional balance of some women – perhaps the majority of women who take it on a long-term basis. Zinc, magnesium, manganese and iron may be deficient in Pill-takers, while copper is often very high. Vitamin A seems to be stored in excess, while many of the B vitamins are in short supply. Some of the adverse side-effects of the Pill have been linked to these changes in vitamin and mineral status. Simply stopping the Pill does not seem to put these nutritional disorders right – they may persist for three months or more and cause continuing problems.

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One line of research into food intolerance has investigated what normally happens to food in the healthy person. There is no reason why the immune system should not attack food molecules just as enthusiastically as it attacks invading germs – after all, food is chemically different from our own bodies, and that is exactly how the immune system recognizes unwelcome aliens.

At one time it was thought that the gut wall rigidly excluded all food molecules, but this is not the case (see p21). In fact the body ‘learns’ not to mount a major immune attack on food. This is done by small areas of the gut wall, known as Peyer’s patches. These patches, which are part of the immune system, take up small droplets of fluid from the gut, in a process known as antigen sampling.

What the Peyer’s patch does is to ‘examine’ the foreign substances it finds in the gut, ‘make a decision’ about how the body should respond to each of them, and ‘communicate’ that decision to the rest of the body. They are rather like immigration officials, alerting the body’s police force (the rest of the immune system) to the arrival of a suspected criminal (a bacterium or virus). But how does the Peyer’s patch distinguish the ‘suspected criminals’ from the ‘innocent holidaymakers’ – in other words, harmless food molecules? No-one knows at present, but the smaller size of food molecules and their lack of ‘stickiness’ is probably important – microbes have a habit of clinging to cell membranes, which is a potential give-away.

Once the Peyer’s patch has recognized a given molecule as food, rather than foe, it tells the body to respond to that molecule in a particular way. It produces a type of cell known as a T-suppressor cell, which is speqific for that molecule and tones down the immune response to it. T-suppressor cells can also influence the type of antibody produced in response to a particular molecule. Some isotypes of antibody produce inflammation when they bind to their antigen (in this case, the food molecule). One isotype does not -it is called immunoglobulin A or IgA and it plays an important part in the body’s response to food.

When microbes get into the blood from the gut, they are met by IgG and IgM antibodies. These bind to their antigen (a molecule on the surface of the microbe) and thus form immune complexes. Once bound, both IgG and IgM summon the body’s defensive forces for an all-out attack, which may cause local damage to the body’s own tissues, seen as inflammation. IgA is different – it has a ‘softly softly’ approach. Although it binds to its target to form immune complexes, it does not provoke inflammation. Circulating immune complexes containing IgA are mopped up by phagocytes or ‘eating cells’ – the body’s garbage-disposal team – without any fuss.

It will be clear that IgA is the ideal antibody for disposing of food molecules which accidentally make it through to the bloodstream. One effect of the Peyer’s patches is to tell the body to form more IgA to food molecules, and less IgG, so that the immune complexes produced are less inflammatory. This process is called the induction of oral tolerance.

The idea that this process breaks down in food intolerance is an attractive one. At present, there is some evidence to support it, but not a great deal. It does seem, however, that patients with food intolerance make more IgG to food molecules,in the blood, and less IgA. They may also produce some IgE, so that the immune complexes could trigger off mast cells.

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If defective genes lead to allergy then one would expect most allergies to begin early in life, as indeed they do. Symptoms cannot be produced the first time a person is exposed to an allergen, however. Although the body already has the capacity to produce antibody to the allergen concerned (in the form of as-yet-unactivated B cells) the antibody itself is not there. An initial exposure is required to enable the body to ‘find’ the right B cell from its extensive stock and multiply it up to useful levels. Once this has happened, a second exposure to the allergen can stimulate antibody (IgE) production. The allergen can then trigger off IgE-coated mast cells with devastating results.

Despite this, a baby may react to a food allergen the first time he eats it because molecules of the food may have reached him by other means. One such route is breast milk, which contains molecules from the foods the mother herself is eating – only a few, of course, but enough to sensitize a highly atopic baby. Some babies may even be sensitized before birth, by food molecules in the mother’s blood that pass into the foetus’s blood. So it is important for atopic mothers-to-be to think about their diet. Chapter Thirteen suggests practical steps that can be taken by parents to reduce the risk of sensitizing their children.

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